Follistatin 344 and ACE-031 are two molecules described as myostatin blockers, myostatin being the protein that limits muscle growth in the body. Follistatin binds myostatin and related ligands; ACE-031 works as a decoy receptor that captures them. Neither has randomised human trials confirming a gain in muscle mass.
ACE-031 was studied in boys with Duchenne muscular dystrophy, but the programme was halted for safety reasons. This article explains how these molecules were meant to work and why the data are so thin. The broader context is set out in the pillar article on muscle peptides, the IGF-1 axis and myostatin.
What is myostatin?
Myostatin, also designated GDF-8, is a protein of the TGF-beta superfamily that restrains the growth of skeletal muscle. Animals and people carrying a mutation that switches off the myostatin gene have markedly greater muscle mass. That observation is the basis for the idea of blocking the protein pharmacologically.
How is follistatin 344 supposed to work?
Follistatin is a secreted protein that binds ligands of the TGF-beta superfamily, myostatin among them, and in doing so lifts the brake on muscle growth. The number 344 refers to one of the variants of the molecule. The spectacular results attributed to follistatin, however, come from mice lacking the myostatin gene. Those animals have a different muscle physiology from animals and people with a normal gene, so the results cannot be carried across directly.
How is ACE-031 supposed to work?
ACE-031 is a fusion protein built from the activin receptor type IIB joined to an antibody fragment. It acts as a decoy receptor: it captures myostatin, activin A, activin B and related molecules before they reach muscle cells. In the muscular dystrophy trials this was meant to support muscle growth and repair.
Why were the ACE-031 trials stopped?
For safety reasons. Acceleron Pharma and Shire suspended the ACE-031 trials in Duchenne muscular dystrophy on 21 April 2011, and on 2 May 2013 they closed the programme altogether and never restarted it. Some participants developed nosebleeds and bleeding gums along with small dilated blood vessels in the skin. The symptoms resolved after the drug was withdrawn. They were linked to the blocking of BMP9 and BMP10 signalling by the activin receptor, signals that matter for the normal functioning of blood vessels.
What does this mean for a buyer?
For follistatin 344 and ACE-031 there is no clinical data confirming effectiveness for building muscle in healthy people, and the only substantial research programme on a myostatin blocker was closed because of adverse effects. In this shop both are stocked strictly as research material: follistatin 344 and ACE-031. The terms of purchase are set out on the legal warning page.
Frequently asked questions
Does follistatin 344 build muscle in humans?
There are no randomised trials showing that. The spectacular results come from mice lacking the myostatin gene, and those animals have a different muscle physiology from humans.
What is the difference between follistatin and ACE-031?
Follistatin is a protein that binds myostatin and related ligands. ACE-031 is a fusion protein acting as a decoy receptor, capturing the same molecules before they reach the cells.
Is ACE-031 safe?
The ACE-031 research programme was closed in 2013 because of adverse effects: nosebleeds, bleeding gums and dilated vessels in the skin.
Are these molecules approved medicines?
They are not. Neither follistatin 344 nor ACE-031 has been approved for any indication.
Where this information comes from
The statement that follistatin has no randomised human trials for muscle gain, and that the results come from mice lacking the myostatin gene, comes from a Know Your Peptide guide of July 2026. The description of ACE-031 as an activin receptor fusion protein, the suspension of trials on 21 April 2011, the closure of the programme on 2 May 2013 and the vascular symptoms come from an article of the Muscular Dystrophy Association dated 2 May 2013. Linking those symptoms to the blocking of BMP9 and BMP10 comes from material describing the mechanism of the activin receptor type IIB. These pages were checked on 31 August 2026.